期刊
VIROLOGY JOURNAL
卷 10, 期 -, 页码 -出版社
BMC
DOI: 10.1186/1743-422X-10-317
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资金
- NIH [AI43000]
- Louisiana Board of Regents Governor's Biotechnology Initiative grant
- Support Cores of the Center for Experimental Infectious Disease Research
- NIH:NIGMS [P20GM103458]
- NIH: NIGMS [P20GM103458]
Background: Herpes simplex virus type-1(HSV-1) and HSV-2 are important human pathogens that cause significant ocular and urogenital complications, respectively. We have previously shown that HSV-1 virions lacking glycoprotein K (gK) are unable to enter into neurons via synaptic axonal membranes and be transported in either retrograde or anterograde manner. Here, we tested the ability of HSV-1 (F) gK-null to protect against lethal challenge with either highly virulent ocular HSV-1 (McKrae strain), or genital HSV-2 (G strain). The gK-null virus vaccine efficiently protected mice against lethal vaginal infection with either HSV-1(McKrae) or HSV-2 (G). Results: Female mice were immunized via a single intramuscular injection with 10(6) PFU of the gK-null virus. Immunized mice were treated with DepoProvera fourteen days after vaccination and were challenged via the vaginal route one week later. Ninety percent of mice vaccinated with the gK-null virus survived HSV-1 (McKrae) challenge, while 70% of these mice survived after HSV-2 (G) challenge. Moreover, all vaccinated mice exhibited substantially reduced disease symptoms irrespective of HSV-1 or HSV-2 challenge as compared to the mock vaccinated challenge group. T-cell memory immune responses to specific glycoprotein B (gB) and glycoprotein D (gD) peptide epitopes were detectable at 7 months post vaccination. Conclusions: These results suggest that the highly attenuated, nonneurotropic gK-null virus may be used as an effective vaccine to protect against both virulent HSV-1 and HSV-2 genital infections and induce lasting immune responses.
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